Subject: Liburdy on Melatonin...... (fwd)
Date: Sat, 16 May 1998 124154 -0500 (CDT)
From: "Roy L. Beavers" <rbeavers@llion.org>
To: emfguru@hotmail.com
--------------------------------------------------
Hi everybody:
I am in receipt of the latest EMF RAPID "Breakout Group Reports for
Epidemiological Research Findings," a final report of the symposium
which was held in San Antonio, Texas, January 12-14, 1998.
Actually, in this message I am forwarding only a portion of the results
of the San Antonio meeting: 'quoted segments' of a paper prepared
by Dr. Robert Liburdy, PhD, of the Lawrence Berkeley National Laboratory.
Liburdy's paper is attached as "Appendix One" to the final report
of the meeting. (It is actually an addendum to the discussion report of
"Role of Mechanistic Data in Strengthening the Epidemiology Findings."
This was one of the breakout groups at the meeting.)
Knowing of the high level of interest within this group concerning the
Melatonin Thesis, and because I consider that what follows from Liburdy's
paper is "state of the art" on the subject, I quote at length below from
that paper. It reflects much of what was discussed in the breakout
group at the meeting, where I also was present and can attest to the fact
that this information was presented and discussed (generally) as reported
here by Dr. Liburdy.
Liburdy's paper is too long for me to include all of it below. In
selecting the quotations I have (below), I am trying to give you as much
of the 'flavor' as possible -- because there is important new information
here about the Melatonin Thesis!
I do not have good fax capabilities. Those of you who may want the
complete document should e-mail Mary Wolfe at NIEHS,
.
What follows is quoted directly from Liburdy's paper. I am omitting
quotation marks and the numerous references he cites within his text. I
will comment briefly at the end....
Cheerio.......
Roy Beavers (EMFguru)
rbeavers@llion.org..............http://www.feb.se/EMF-L/EMF-L.html
................................It is better to light a single candle ...
than to curse the darkness...............................................
Submitted by Robert Liburdy, Ph.D.
The melatonin hypothesis was discussed in detail during the breakout group
discussions. Since the breakout group section reporting on the _in vitro_
studies relating to the melatonin hypothesis did not capture all the
details of the discussion that took place, additional comments are
provided here. For example, the breakout group discussed the action of
EMF on other drugs and chemicals that regulate cell growth, such as
tamoxifen; refer to the figure developed during the discussions. Since
there is no presentation of this research in the report, this material is
provided in this appendix. Literature references for these studies are
listed at the end of the Appendix.
A. _In Vitro evidence for melatonin effects_
A series of studies has shown that EMF exposure as low as 12 mG (1.2 uT)
inhibits melatonin oncostatic activity on MCF-7 breast cancer cells. [refs
skipped.] This work has been independently replicated in two different
laboratories. Thus, three laboratories have independently reported this
bioeffect at 12 mG, and a summary of the results across these three
laboratories with a discussion of the biological and EMF exposure
protocols was presented at the 2nd World Congress for Electricity and
Magnetism in Biology & Medicine; and a manuscript for publication in the
proceedings is in peer-review.
The role that these _in vitro_ findings play in the melatonin hypothesis
was discussed by the breakout group. Demonstration of a direct EMF effect
on the activity or biological activity of the hormone melatonin is a new
finding which modifies the original melatonin hypothesis. The original
hypothesis states that EMF reduces the circulating levels of melatonin,
and this will result in elevated levels of estrogen and prolactin which
increases the risk of breast cancer.
The melatonin hypothesis invokes a general mechanism that has relevance to
all hormone dependent tissue responsive to estrogen and/or prolactin, such
as human mammary epithelial tissue, ovarian tissue, and prostate tissue.
The _in vitro_ findings that EMF can block melatonin's oncostatic action
at the cellular level modifies the melatonin hypothesis and broadens it to
address EMF's effects on melatonin's oncostatic action of target cells.
This has several important consequences.
First, a concomitant reduction in melatonin's oncostatic activity
complements an _in vivo_ reduction in circulating levels of melatonin.
///skip///
Second, it is important to consider the consequences of blocking
melatonin's oncostatic action and how this may act in combination with a
reduction of circulating levels of melatonin. For example, a biological
system's "full response" to EMF could involve both effects to reduce
melatonin's biological activity. In this case, the "target cell" effect
and the "circulation" effect would occur in conjunction to elevate risk of
cancer. However, a reduction in circulating levels of melatonin does not
have to take place for the "target cell" effect to occur. Importantly, in
this case, an EMF effect on reducing melatonin's oncostatic action would
occur in the absence of a reduction in circulating levels of melatonin.
As a result, the melatonin hypothesis is not strictly dependent on a
reduction of circulating melatonin, but is operative when EMF blocks
melatonin's oncostatic activity either a) by an EMF interaction at the
target cell level, b) by an EMF effect on circulating levels of melatonin,
or c) by both interactions.
///skip///
A comment was made by Dr. Liburdy regarding the magnitude of the melatonin
effect on cell proliferation. The experiments conducted by Liburdy,
Blackman, and Luben assessed the effect of melatonin on MCF-7 cells over
one (1) cell division cycle _in vitro_ over approximately seven days of
culture. This is a standard approach for _in vitro_ cell growth studies.
In contradistinction, however, these cells would continue to divide
exponentially _in vivo_ as a tumor mass over many subsequent cell division
cycles. Thus, a change in proliferation of 15-25% for exponentially
growing cells would translate rapidly into a large change in cell numbers
over multiple cell division cycles. In this light, a change in cell
proliferation of 15-25% for exponentially growing cells should be
interpreted as significant within this biological context.
/////skip////
A.1. _In vitro evidence extending the melatonin effect to other growth
regulating drugs and cell types_
Dr. Liburdy commented that tamoxifen is known to inhibit human breast
cancer cell growth, _in vitro_ and _in vivo_, and this action is shown by
the dashed line in the Figure. EMF studies from his laboratory have
recently been reported for the anti-estrogen tamoxifen (Harland & Liburdy,
1997), and these were summarized. In the Figure the tamoxifen pathway
which blocks estrogen growth promotion (dashed line), is inhibited by
magnetic fields ("X" in the Figure). In the tamoxifen experiments MCF-7
cell growth was reduced in a dose-dependent manner by pharmacologically
relevant levels of tamoxifen, and this action was inhibited by 12 mG
magnetic fields. Thus, a second growth regulating compound (tamoxifen)
was inhibited by environmental level EMF. Since tamoxifen is known to act
through the estrogen receptor, these studies suggest that the estrogen
receptor may be involved in this EMF interaction.
////skip////
In summary, the _in vitro_ studies discussed above indicate that
environmental level magnetic fields can block or inhibit the action of
several growth regulating compounds that act through the estrogen
receptor, as well as the hormone melatonin. These effects have been
observed in two human breast cancer cell lines (ER+): MCF-7 and T47D
cells. Further studies are required to identify specific, underlying
biological mechanisms of action, and to extend these findings to
additional cell types.
**************************************************
A brief commentary from guru.......
The two-pronged attack of EMF exposure upon human cell activity reported
by Dr. Liburdy (above) constitutes the strongest evidence so far that
the melatonin hypothesis provides _at least one_ STRONG "mechanism"
explanation for what is being found in the epidemiology studies.....
I do not believe that melatonin will prove to be the "only" one. And I do
not claim that it is "the most basic mechanism." We are not likely to
ever see that: the action of the electrons in either "resonating with" or
"disrupting" other electrons thereby resulting in chemical activity.
What we are beginning to see is the chemical activity.....
The "science community" studying this issue (except for a few more daring
souls) is still not willing to credit this ***three times replicated***
evidence as "definitive" of an EMF health hazard..... That is evident to
me by the "waffling" verbiage appearing in the reports that are coming
out of this EMF RAPID review effort.
Question: Who was it that ever started public policy down the road of
requiring a "definitive" standard of "proof" before government and others
(like the medical community) can begin to institute protective policies
on behalf of the public??? ... And, equally important, tell the truth to
the public about what WE DO KNOW!!!.....
Many of us on this list believe we know the answer. It was the vested
interests...... They are not the ones to define the way public policy
should be made on these matters. Not in the case of lead or tobacco or
EMF. And it is well nigh time that a new standard -- more protective of
public health considerations -- be thrust into the public policy
decision-making machinery.
This requires that the public be given the truth...... Then the public
will DEMAND action in their interest rather then in the industry's
interest.
Frankly, it is my observation (after nearly five years exposure to the EMF
"science community") that science, by and large, has a great facility for
describing "what we do NOT know" -- but very little facility when it comes
to describing or reporting (to the public and to the government) WHAT WE
DO KNOW........
(I wonder, is that a result of the constant need to justify more research
funding?)
I am informed that we still do not have a "definitive" explanation of
the tobacco hazard _in a scientific sense_. Yes, it has evidently been
formulated (finally) -- and we see it being acted upon -- in a public
health sense. But science still does not know all the "mechanisms" that
explain tobacco's harmful biological action.....
This "hang-up" that we are experiencing in arriving at the so-called
"proof" or "definitive findings" of the EMF hazard ... does not do credit
to the substantial gains in our knowledge that have come about over the
past five years.
We now KNOW, for example, that biological activity can occur as a
consequence of EMF exposure levels which are present in our environment.
We have replicated evidence that at least one of the responsible
mechanisms has been identified -- melatonin and the estrogen
receptors.....
We owe some special thanks to the likes of Liburdy, Blackman, Luben...
for the work they have done on the melatonin thesis over the past five
years. We are also greatly indebted to Richard Stevens of Battelle
Laboratory for "seeing through the fog" of this EMF mystery as early as
1985 and putting forth the "melatonin hypothesis." These men have
required nearly as much courage as wisdom and perseverance to bring
us to the point where we are today......
Are their more of you "out there" of equal courage, wisdom and
perseverance???? You are needed now ... as this matter reaches a
critical junction in the 1998 Report to the Congress......
__________________________________________
P.S. Some time ago, one of this group asked me where I got the idea that
EMF could be a factor in the prostate cancer surge now being seen in
industrial countries???? It's there ... in the text of Dr. Liburdy's
paper......
Cheerio......
Roy Beavers(EMFguru)
Archive provided courtesy of WaveGuide, http://www.wave-guide.org
Reprinted with permission of Roy Beavers, http://www.feb.se/EMF-L/EMF-L.html